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BIOL2016 - Pharmacology > NMJ > Flashcards

NMJ Flashcards

1
Q

What does the somatic nervous system activate?

A

Skeletal muscle contraction

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2
Q

How is the somatic nervous system regulated?

A

By corticospinal tracts and spinal reflexes

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3
Q

Somatic synapses?

A

One at NMJ - ACh –> nicotinic receptor

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4
Q

Parasympathetic synapses?

A

Long preganglionic - ACh –> nicotinic receptor

Short postganglionic - ACh –> muscarinic receptor

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5
Q

Sympathetic synapses?

A

Short preganglionic - ACh –> nicotinic receptor
Long postganglionic - NE –> adrenergic receptors

(sweat glands ACh –> muscarinic)

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6
Q

What does the autonomic nervous system activate?

A

Smooth muscle
Exocrine glands
Cardiac tissue
Metabolic activities

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7
Q

How is the autonomic nervous system regulated?

A

By brain stem centres

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8
Q

Outline the structure of a nicotinic receptor

A

Ligand gated ion channel
Requires the binding of 2 ACh molecules.
5 subunits.

Upon binding, the 2nm channel opens wider due to conformational changes.

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9
Q

Composition of NM/N1 form?

A

a1 x 2
b1
delta
epsilon (gamma in embryonic)

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10
Q

Composition of NN/N2 form?

A

a2-10

b2-4

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11
Q

What is the NMJ?

A

Specialised form of synaptic transmission between neurons and skeletal muscle to cause muscle contraction

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12
Q

What causes the release of neurotransmitter?

A

Motor neuron depolarisation causes the action potential to travel down the nerve fibre to the NMJ.
Depolarisation of the axon terminal causes an influx of Ca2+
Triggers fusion of synaptic vesicles and release of ACh (neurotransmitter)

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13
Q

What does the neurotransmitter cause?

A

ACh binds to postsynaptic ACh receptor on the muscle fibre at the motor end plate
Binding opens the channels, causing an influx of sodium ions.
Depolarisation occurs on the sarcolemma and travels down the T tubules to cause the release of Ca2+ from the sarcoplasmic reticulum - contraction

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14
Q

What happens to the ACh?

A

Ubound ACh diffuses away or is hydrolysed by AChE

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15
Q

Outline Myasthenia gravis?

A

Autoantibodies to the nicotinic ACh receptors on the motor end plates of muscles. Binding of ACh is blocked. Also induce complement-mediated degradation of the receptors, resulting in progressive weakening of the skeletal muscles.

Autoantibodies to MuSK which is important for the tight clustering of receptors at the NMJ

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16
Q

Symptoms of Myasthenia gravis?

A

Weakness of eye muscles, swallowing and slurred speech.

Eye movement, facial expressions, chewing, talking, swallowing.

Breathing and neck movements.

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17
Q

Describe Lambert-Eaton myasthenic syndrome?

A

Autoantibodies to presynaptic voltage gated calcium channel (VGCC)

Interfere with the calcium dependent release of ACh from the presynaptic membrane and cause a reduced endplate potential on the postsynaptic membrane

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18
Q

Describe Neuromyotonia (Isaac’s syndrome)?

A

Autoantibodies to presynaptic voltage gated potassium channels (VGKC).
Results in continuous excitability.

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19
Q

Main drugs involved at NMJ?

A

ACh blocking agents

Anticholinesterases (increases ACh - all others block/decrease)

Drugs affecting synthesis and storage of axonal ACh

20
Q

Active compound in curare?

A

d-tubocararine
skeletal muscle paralysis
blocks ACh binding to the receptor

Non depolarising blocking agent.

21
Q

Subclasses of neuromuscular blocking drugs?

A

Depolarising and non-depolarising

22
Q

Mechanism of non depolarising blockers?

A

Prevents the opening of the channel when it competitively binds to the receptor.
Can be reversed.

23
Q

Rocuronium?

A

Non depolarising blocker

24
Q

Mechanism of depolarising blockers?

A

Occupy the receptor site, opening the channel and block the channel.
Normal closure of the gate is prevented and the blocker can move into the pore.
May desensitise the end plate by causing persistent depolarisation

25
Q

Succinylcholine?

A

Depolarising blocker

26
Q

Cobratoxin and a-bungarotoxin?

A

Bind with high affinity to the nicotinic receptors, causing a postsynaptic block at the NMJ

27
Q

Effects of NMJ blocking agents?

A

Paralysis from the small rapidly moving muscles to limbs then respiratory muscles

28
Q

Non depolarising agents effect?

A

Flaccid, relaxed paralysis.
Can be reversed by AChE inhibitors.
Histamine release.
Muscarinic blocking.

29
Q

Depolarising agents effect?

A

Phase 1 - membrane depolarisation, transient fasiculations –> paralysis

Phase 2 - desensitisation. Membrane depolarises and is hypersensitive to ACh. Block can’t be reversed

30
Q

Pancuronium?

A

Non depolarising blocking agent

31
Q

Gallamine?

A

Non depolarising blocking agent

32
Q

Mlvacurium?

A

Non depolarising blocking agent

33
Q

Atracurium?

A

Non depolairising blocking agent

34
Q

Clinical uses of NMJ blocking agents?

A 
Muscle relaxation in surgety 
Orthopedics 
Facilitate intubations
Facilitate internal exams
Prevent trauma 
Diagnostic
35
Q

Uses of acetylcholinesterase inhibitors?

A 
Myasthenia gravis treatment 
Alzheimer's
Lewy body dementia 
Glaucoma 
Antidote for anticholinergic poisoning
36
Q

Types of acetylcholinesterase inhibitors?

A

Venoms & poisons

Nerve agents & insecticides

37
Q

Examples of acetylcholinesterase inhibitors?

A

Edrophonium
Neostigmine
Pyridostigmine
Distigime

38
Q

Symptoms of NMJ overstimulation?

A 
Vasodilation
Sweating
Salivation
Bronchial secretions
Miosis 
Flaccid paralysis
Respiratory failure.
39
Q

Nerve gas poisoning?

A

Atropine - antidote, blocks ACh from binding

Oximes can regenerate the enzymes

40
Q

Organophosphates?

A

Irreversible acetylcholinesterase inhibitors
phosphorus atom covalently binds to a serine hydroxyl group in the active site

pralidoxime reactives the enzmye

41
Q

Neostigmine?

A

AChE inhibitor which permits buildup of ACh for more intensive and prolonged activation.

Time prolonged to interact with receptors that are not blocked by autoantibodies

42
Q

Edrophonium?

A

Readily reversible AChE inhibitor.
True competitive inhibition.
Can be used to differentiate myasthenic from cholinergic crisis.

43
Q

Myasthenic crisis?

A

Not enough NM stimulation.

Edrophonium will reduce muscle weakness by supplying more ACh

44
Q

Cholinergic crisis?

A

Too much NM stimulation.

Will make weakness worse by inducing a depolarising block.

45
Q

Physostigmine?

A

Reversible pseudocompetitive AChE inhibitor.

Treat myasthenia gravis, Alzheimer’s and delayed gastrice emptying

Crosses BBB

46
Q

AChE inhbitors to treat dementia?

A

hypothesis - cognitive decline is linked to hippocampus and cortex.

47
Q

SNARE proteins?

A

allow vesicles to release AC into NMJ.

Botox cleaves specific SNARE proteins to block the vesicles from releasing ACh.

BIOL2016 - Pharmacology (6 decks)

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